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Endoscopic Removal of Pharmacobezoar in Case of Intentional Potassium Overdose
The Journal of Emergency Medicine, Vol. 46, No. 3, pp. 351–354, 2014 Copyright Ó 2014 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$ - see front matter
http://dx.doi.org/10.1016/j.jemermed.2013.08.031
Selected Topics: Toxicology
ENDOSCOPIC REMOVAL OF PHARMACOBEZOAR IN CASE OF INTENTIONAL POTASSIUM OVERDOSE Albert L. Briggs, MD* and Lisa L. Deal, PHARMD, BCPS*† *Department of Emergency Medicine, Carilion Roanoke Memorial Hospital, Roanoke, Virginia and †Department of Pharmacy, Carilion Roanoke Memorial Hospital, Roanoke, Virginia Reprint Address: Lisa L. Deal, PHARMD, BCPS, Departments of Emergency Medicine and Pharmacy, Carilion Clinic, Carilion Roanoke Memorial Hospital, 1906 Belleview Avenue, Roanoke, VA 24014
, Keywords—overdose; potassium chloride; pharmacobezoar; EGD
, Abstract—Background: Hyperkalemia is a potentially life-threatening electrolyte abnormality commonly seen in the emergency department (ED). Intentional overdose of potassium supplements is an uncommon occurrence. Objective: This case illustrates a novel approach to treatment of pharmacobezoar with esophagogastroduodenoscopy (EGD) and demonstrates its effectiveness in the setting of extended-release potassium chloride overdose. Case Report: A 44-year-old female presented to the ED with intentional ingestion of an unknown amount of extended-release potassium chloride (K-DurÒ) tablets and alprazolam (XanaxÒ). The patient’s serum potassium was initially 7.3 mmol/L and she was treated with standard treatments, including albuterol, calcium gluconate, insulin, dextrose, and sodium bicarbonate. Radiographic investigation showed a pharmacobezoar in the gastric fundus. Treatment was then augmented with whole bowel irrigation (WBI) using polyethylene glycol solution via nasogastric tube. Patient did not tolerate the nasogastric tube, became combative with increasing alteration in her level of consciousness, and WBI therapy was stopped. After discussion with the gastroenterologist, the patient was treated with EGD to remove the pharmacobezoar. The EGD was successful in the removal of the pharmacobezoar and the patient’s potassium normalized without complications. Conclusions: We recommend that in cases of suspected or confirmed potassium drug bezoar in the stomach, physicians consider EGD for removal. This allows for normalization of potassium level while preventing adverse sequelae. Ó 2014 Elsevier Inc.
INTRODUCTION Hyperkalemia is a common finding in emergency department (ED) patients. Severe hyperkalemia has the potential to cause life-threatening cardiac dysrhythmias. Intentional overdose of oral potassium supplements infrequently causes hyperkalemia in previously healthy patients with normal renal function (1,2). Hyperkalemia associated with oral potassium supplement use is most commonly seen in individuals with impaired renal function or in patients taking medications that influence potassium metabolism. Pharmacobezoar formation occurs rarely and has not been previously reported in cases of potassium supplement ingestion. We report the case of a patient with normal renal function who developed severe hyperkalemia due to oral potassium supplement ingestion, complicated by potassium-containing pharmacobezoar treated by endoscopic removal. CASE REPORT A 44-year-old female nurse with a history of anxiety disorder presented to the ED at approximately 1:15 pm after ingesting a potassium supplement and alprazolam
RECEIVED: 1 December 2012; FINAL SUBMISSION RECEIVED: 1 May 2013; ACCEPTED: 14 August 2013 351
352
at home. She believed that her potassium was low and was trying to increase her level by taking extra potassium tablets. She stated this was not a suicide attempt. She gave differing accounts to staff and providers about the amount of pills ingested and time of ingestion. The total theoretical amount of potassium ingested would have been 600 mEq (thirty 20-mEq tablets) of potassium chloride extended-release preparation (K-DurÒ) and 60 mg (sixty 1-mg tablets) of alprazolam based on prescription refill data provided by the patient’s pharmacy. On arrival to the ED, the patient’s blood pressure was 89/59 mm Hg, pulse was 82 beats/min, respirations were 20 breaths/min, temperature was 36.5 C, and oxygen saturation was 100% on room air. Her abdomen was soft and nontender. Skin was warm and dry. On neurologic examination, she was oriented to person, place, and time and conversant with staff. A 12-lead electrocardiogram demonstrated normal sinus rhythm with normal QRS duration and mildly peaked T-waves (Figure 1). Potassium level was 7.3 mmol/L. Creatinine was 0.69 mg/dL. Plain film of the abdomen revealed a 4-cm oval density in the region of the gastric fundus (Figure 2). Standard toxicological screen was positive for benzodiazepines, but negative for all other agents, including acetaminophen and salicylates. Ethanol level was negative. Treatment for hyperkalemia was initiated, including 15 mg/h of continuous aerosolized albuterol, 1 g i.v. calcium gluconate, 10 U i.v. regular insulin with 25 g i.v. dextrose, and 50 mEq i.v. sodium bicarbonate. The radiographic finding of the density in the region of the gastric fundus raised suspicion of a pharmacobezoar
A. L. Briggs and L. L. Deal
containing potassium. A nasogastric (NG) tube was placed and whole bowel irrigation (WBI) therapy was initiated with polyethylene glycol-electrolyte solution (PEG-ES). Thirty minutes after receiving the first liter of bowel irrigant, the patient became combative, pulled out her NG tube, and would not allow re-insertion. Her mental status declined, requiring verbal stimulation to maintain wakefulness. Repeat potassium levels showed improvement with decrease to 6.0 mmol/L 2 h after ED arrival, but subsequently rebounded to 6.7 mmol/L 4 h after presentation. Consultation with the gastroenterology service was made to request esophagogastroduodenoscopy (EGD) for removal of suspected pharmacobezoar. The patient was taken to the endoscopy suite 6 h after arrival, where she was intubated for the procedure with 100 mg propofol and remained sedated with a propofol infusion titrated to light sedation. During the procedure, a granular slurry of medication was removed with dry suction, followed by rapid irrigation and suction cycles until all visible remnants of drug were removed from the stomach (Figure 3). The scope was passed into the duodenum and no medication was visible (Figure 4). No other abnormal findings were noted. She was transferred to the intensive care unit, where potassium levels normalized after endoscopy, 11 h after ED arrival. She was extubated 12 h after the EGD and discharged to the psychiatry service the following day. DISCUSSION Hyperkalemia is frequently seen in ED patients, commonly those suffering from renal failure and in patients
Figure 1. Initial electrocardiogram on arrival to emergency department.
Pharmacobezoar with Potassium Overdose
Figure 2. Kidney, ureter, and bladder (KUB) radiograph with density in gastric fundus without discrete pill fragments.
on medications that affect potassium homeostasis. Medications that influence potassium metabolism include potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, digoxin, and nonsteroidal anti-inflammatory agents (3,4). Hyperkalemia due to intentional overdose of potassium supplement is rare. In patients with normal renal function the oral ingestion of potassium would have to overwhelm the kidney’s excretory ability in order to become problematic. Pharmacobezoar formation due to drug ingestion occurs infrequently and has not been reported in cases of potassium supplement ingestion. Pharmacobezoars are classified into four types: phytobezoars, trichobezoars,
Figure 3. Esophagogastroduodenoscopy photo of pharmacobezoar containing extended-release potassium chloride and alprazolam.
353
Figure 4. Esophagogastroduodenoscopy photo after irrigation and removal of extended-release potassium chloride pharmacobezoar.
lactobezoars, and pharmacobezoars. Bezoar formation can be increased in patients with alterations in gastric physiology, including partial gastrectomies and vagotomies. Guillain-Barre syndrome, diabetes, and cystic fibrosis have also been implicated in bezoar development (5). Pharmacobezoars are more commonly associated with extended-release preparations. The coating in this type of preparation is a semi-permeable membrane that allows for continuous, controlled release of medication over a time period (5). K-DurÒ is an extended-release potassium tablet that contains coated potassium chloride micropellets. The coating is composed of ethylcellulose and hydroxypropylcellulose (6). The inert ingredients include crospovidone and magnesium stearate. Magnesium stearate is a hydrophobic material that can change the rate of dissolution and may potentiate bezoar formation due to changes in dispersion of the tablet (7,8). Once ingested, the potassium chloride tablet dissolves and releases the micropellets. The micropellets will release the potassium chloride slowly over 8 10 h, preventing high gastric concentrations of potassium and reducing gastrointestinal upset with therapeutic use (6). The bezoar formation in this case is likely related to the inert ingredients in the potassium chloride tablet confounded by the number of tablets that altered the pH and prevented tablet degradation and micropellet release. EGD is not routinely advocated as treatment for acute drug ingestions. It has, on rare occasions, been used to remove pharmacobezoars, however, not in cases of potassium ingestion (9 11). Markedly elevated potassium levels can cause life-threatening cardiac dysrhythmias. The goals of therapy are threefold: raise the threshold for cardiac
354
A. L. Briggs and L. L. Deal
dysrhythmias, shift potassium into the cell, and remove potassium from the body (12). The medical therapy for hyperkalemia, whether it is due to renal insufficiency; prescription medication related; or intentional overdose, is the same, with the added consideration of gastrointestinal decontamination in cases of overdose. WBI with PEG-ES has been reported to be a successful means of removing potassium tablets remaining in the gastrointestinal tract (2,13 15). In our patient, WBI was commenced but was not completed due to combativeness and declining mental status, as the patient was not able to tolerate oral administration and she refused repeated insertion of the NG tube. The change in mental status was believed to be due to coingestion of benzodiazepines. Consideration was given to more aggressive attempts at WBI with airway protection, however, there was concern about the ability of WBI to eliminate the radiographically apparent pharmacobezoar. With this in mind, the decision was made to pursue endoscopic removal. The patient underwent successful removal of a pharmacobezoar with improvement in potassium levels. Serum potassium level of 4.5 mmol/L was obtained approximately 11 h after ED arrival. She was extubated after the procedure and monitored in the intensive care unit. To our knowledge, this is the first report of successful endoscopic removal of a potassium chloride pharmacobezoar. The pharmacobezoar may have increased the risk of the hyperkalemia due to the erratic and prolonged absorption of the potassium. Co-ingestion of substances or drugs that delay gastric emptying like alprazolam may promote bezoar formation. We recommend that in cases of suspected or confirmed potassium drug bezoar in the stomach, physicians consider EGD for removal. This allows for normalization of potassium levels and obviates the need for prolonged intubation to protect the airway in case of prolonged WBI. CONCLUSIONS This was a case of intentional potassium and alprazolam overdose resulting in hyperkalemia with normalization
of potassium levels after utilizing both potassiumlowering medications and EGD. Although intentional overdose with potassium supplementation is rare, bezoar formation can lead to prolonged and erratic absorption of potassium and increase the risk of hyperkalemic sequelae. In addition to standard treatments for hyperkalemia, our case report demonstrates the benefit from EGD in extended-release potassium bezoar formation. REFERENCES 1. John SK, Rangan Y, Block C, Koff M. Life-threatening hyperkalemia from nutritional supplements: uncommon or undiagnosed? Am J Emerg Med 2011;29:1237e1–2. 2. Su M, Stork C, Ravuri S, et al. Sustained-release potassium chloride overdose. Clin Toxicol 2001;39:641–8. 3. Hollander-Rodriguez JC, Calvert JF. Hyperkalemia. Am Fam Phys 2006;73:283–90. 4. Evans KJ, Greenberg A. Hyperkalemia: a review. J Intensive Care Med 2005;20:272–89. 5. Sanders MK. Bezoars: from mystical charms to medical and nutritional management. Pract Gastroenterol 2004;13:37–50. 6. Rogers LR, Wallick D. Reviewing the use of ethylcellulose, methylcellulose and hypromellose in microencapsulation. Part 1: materials used to formulate microcapsules. Drug Dev Indust Pharm 2012;38:129–57. 7. Samyn JC, Jung WY. In vitro dissolution from several experimental capsule formations. J Pharm Sci 1970;59:169–75. 8. Murthy KS, Samyn JC. Effect of shear mixing on in vitro drug development of capsule formulations containing lubricants. J Pharm Sci 1977;66:1215–9. 9. Ng HW, Tse ML, Lau FL, Chu W. Endoscopic removal of iron bezoar following acute overdose. Clin Toxicol 2008;46:913–5. 10. Hojer J, Personne M. Endoscopic removal of slow release clomipramine bezoars in two cases of acute poisoning. Clin Toxicol 2008; 46:317–9. 11. Wells CD, Luckritz TC, Rady MY, et al. Bezoar formation requiring endoscopic removal after intentional overdose of extended-release nifedipine. Pharmacotherapy 2006;26:1802–5. 12. Elliott MJ, Ronksley PE, Clase CM, et al. Management of patients with acute hyperkalemia. CMAJ 2010;182:1631–5. 13. American Academy of Clinical Toxicology. European Association of Poison Centres and Clinical Toxicologists. Position paper: whole bowel irrigation. J Toxicol Clin Toxicol 2004; 42:843–54. 14. Whitaker RJ, Maguire JE. Slow-release potassium overdose: clinical features and the role of whole-bowel lavage in management. Emerg Med 2000;12:218–25. 15. Wan CK, Tong HK. A case of slow-release potassium chloride overdose. Hong Kong J Emerg Med 2007;14:169–73.
http://dx.doi.org/10.1016/j.jemermed.2013.08.031
Selected Topics: Toxicology
ENDOSCOPIC REMOVAL OF PHARMACOBEZOAR IN CASE OF INTENTIONAL POTASSIUM OVERDOSE Albert L. Briggs, MD* and Lisa L. Deal, PHARMD, BCPS*† *Department of Emergency Medicine, Carilion Roanoke Memorial Hospital, Roanoke, Virginia and †Department of Pharmacy, Carilion Roanoke Memorial Hospital, Roanoke, Virginia Reprint Address: Lisa L. Deal, PHARMD, BCPS, Departments of Emergency Medicine and Pharmacy, Carilion Clinic, Carilion Roanoke Memorial Hospital, 1906 Belleview Avenue, Roanoke, VA 24014
, Keywords—overdose; potassium chloride; pharmacobezoar; EGD
, Abstract—Background: Hyperkalemia is a potentially life-threatening electrolyte abnormality commonly seen in the emergency department (ED). Intentional overdose of potassium supplements is an uncommon occurrence. Objective: This case illustrates a novel approach to treatment of pharmacobezoar with esophagogastroduodenoscopy (EGD) and demonstrates its effectiveness in the setting of extended-release potassium chloride overdose. Case Report: A 44-year-old female presented to the ED with intentional ingestion of an unknown amount of extended-release potassium chloride (K-DurÒ) tablets and alprazolam (XanaxÒ). The patient’s serum potassium was initially 7.3 mmol/L and she was treated with standard treatments, including albuterol, calcium gluconate, insulin, dextrose, and sodium bicarbonate. Radiographic investigation showed a pharmacobezoar in the gastric fundus. Treatment was then augmented with whole bowel irrigation (WBI) using polyethylene glycol solution via nasogastric tube. Patient did not tolerate the nasogastric tube, became combative with increasing alteration in her level of consciousness, and WBI therapy was stopped. After discussion with the gastroenterologist, the patient was treated with EGD to remove the pharmacobezoar. The EGD was successful in the removal of the pharmacobezoar and the patient’s potassium normalized without complications. Conclusions: We recommend that in cases of suspected or confirmed potassium drug bezoar in the stomach, physicians consider EGD for removal. This allows for normalization of potassium level while preventing adverse sequelae. Ó 2014 Elsevier Inc.
INTRODUCTION Hyperkalemia is a common finding in emergency department (ED) patients. Severe hyperkalemia has the potential to cause life-threatening cardiac dysrhythmias. Intentional overdose of oral potassium supplements infrequently causes hyperkalemia in previously healthy patients with normal renal function (1,2). Hyperkalemia associated with oral potassium supplement use is most commonly seen in individuals with impaired renal function or in patients taking medications that influence potassium metabolism. Pharmacobezoar formation occurs rarely and has not been previously reported in cases of potassium supplement ingestion. We report the case of a patient with normal renal function who developed severe hyperkalemia due to oral potassium supplement ingestion, complicated by potassium-containing pharmacobezoar treated by endoscopic removal. CASE REPORT A 44-year-old female nurse with a history of anxiety disorder presented to the ED at approximately 1:15 pm after ingesting a potassium supplement and alprazolam
RECEIVED: 1 December 2012; FINAL SUBMISSION RECEIVED: 1 May 2013; ACCEPTED: 14 August 2013 351
352
at home. She believed that her potassium was low and was trying to increase her level by taking extra potassium tablets. She stated this was not a suicide attempt. She gave differing accounts to staff and providers about the amount of pills ingested and time of ingestion. The total theoretical amount of potassium ingested would have been 600 mEq (thirty 20-mEq tablets) of potassium chloride extended-release preparation (K-DurÒ) and 60 mg (sixty 1-mg tablets) of alprazolam based on prescription refill data provided by the patient’s pharmacy. On arrival to the ED, the patient’s blood pressure was 89/59 mm Hg, pulse was 82 beats/min, respirations were 20 breaths/min, temperature was 36.5 C, and oxygen saturation was 100% on room air. Her abdomen was soft and nontender. Skin was warm and dry. On neurologic examination, she was oriented to person, place, and time and conversant with staff. A 12-lead electrocardiogram demonstrated normal sinus rhythm with normal QRS duration and mildly peaked T-waves (Figure 1). Potassium level was 7.3 mmol/L. Creatinine was 0.69 mg/dL. Plain film of the abdomen revealed a 4-cm oval density in the region of the gastric fundus (Figure 2). Standard toxicological screen was positive for benzodiazepines, but negative for all other agents, including acetaminophen and salicylates. Ethanol level was negative. Treatment for hyperkalemia was initiated, including 15 mg/h of continuous aerosolized albuterol, 1 g i.v. calcium gluconate, 10 U i.v. regular insulin with 25 g i.v. dextrose, and 50 mEq i.v. sodium bicarbonate. The radiographic finding of the density in the region of the gastric fundus raised suspicion of a pharmacobezoar
A. L. Briggs and L. L. Deal
containing potassium. A nasogastric (NG) tube was placed and whole bowel irrigation (WBI) therapy was initiated with polyethylene glycol-electrolyte solution (PEG-ES). Thirty minutes after receiving the first liter of bowel irrigant, the patient became combative, pulled out her NG tube, and would not allow re-insertion. Her mental status declined, requiring verbal stimulation to maintain wakefulness. Repeat potassium levels showed improvement with decrease to 6.0 mmol/L 2 h after ED arrival, but subsequently rebounded to 6.7 mmol/L 4 h after presentation. Consultation with the gastroenterology service was made to request esophagogastroduodenoscopy (EGD) for removal of suspected pharmacobezoar. The patient was taken to the endoscopy suite 6 h after arrival, where she was intubated for the procedure with 100 mg propofol and remained sedated with a propofol infusion titrated to light sedation. During the procedure, a granular slurry of medication was removed with dry suction, followed by rapid irrigation and suction cycles until all visible remnants of drug were removed from the stomach (Figure 3). The scope was passed into the duodenum and no medication was visible (Figure 4). No other abnormal findings were noted. She was transferred to the intensive care unit, where potassium levels normalized after endoscopy, 11 h after ED arrival. She was extubated 12 h after the EGD and discharged to the psychiatry service the following day. DISCUSSION Hyperkalemia is frequently seen in ED patients, commonly those suffering from renal failure and in patients
Figure 1. Initial electrocardiogram on arrival to emergency department.
Pharmacobezoar with Potassium Overdose
Figure 2. Kidney, ureter, and bladder (KUB) radiograph with density in gastric fundus without discrete pill fragments.
on medications that affect potassium homeostasis. Medications that influence potassium metabolism include potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, digoxin, and nonsteroidal anti-inflammatory agents (3,4). Hyperkalemia due to intentional overdose of potassium supplement is rare. In patients with normal renal function the oral ingestion of potassium would have to overwhelm the kidney’s excretory ability in order to become problematic. Pharmacobezoar formation due to drug ingestion occurs infrequently and has not been reported in cases of potassium supplement ingestion. Pharmacobezoars are classified into four types: phytobezoars, trichobezoars,
Figure 3. Esophagogastroduodenoscopy photo of pharmacobezoar containing extended-release potassium chloride and alprazolam.
353
Figure 4. Esophagogastroduodenoscopy photo after irrigation and removal of extended-release potassium chloride pharmacobezoar.
lactobezoars, and pharmacobezoars. Bezoar formation can be increased in patients with alterations in gastric physiology, including partial gastrectomies and vagotomies. Guillain-Barre syndrome, diabetes, and cystic fibrosis have also been implicated in bezoar development (5). Pharmacobezoars are more commonly associated with extended-release preparations. The coating in this type of preparation is a semi-permeable membrane that allows for continuous, controlled release of medication over a time period (5). K-DurÒ is an extended-release potassium tablet that contains coated potassium chloride micropellets. The coating is composed of ethylcellulose and hydroxypropylcellulose (6). The inert ingredients include crospovidone and magnesium stearate. Magnesium stearate is a hydrophobic material that can change the rate of dissolution and may potentiate bezoar formation due to changes in dispersion of the tablet (7,8). Once ingested, the potassium chloride tablet dissolves and releases the micropellets. The micropellets will release the potassium chloride slowly over 8 10 h, preventing high gastric concentrations of potassium and reducing gastrointestinal upset with therapeutic use (6). The bezoar formation in this case is likely related to the inert ingredients in the potassium chloride tablet confounded by the number of tablets that altered the pH and prevented tablet degradation and micropellet release. EGD is not routinely advocated as treatment for acute drug ingestions. It has, on rare occasions, been used to remove pharmacobezoars, however, not in cases of potassium ingestion (9 11). Markedly elevated potassium levels can cause life-threatening cardiac dysrhythmias. The goals of therapy are threefold: raise the threshold for cardiac
354
A. L. Briggs and L. L. Deal
dysrhythmias, shift potassium into the cell, and remove potassium from the body (12). The medical therapy for hyperkalemia, whether it is due to renal insufficiency; prescription medication related; or intentional overdose, is the same, with the added consideration of gastrointestinal decontamination in cases of overdose. WBI with PEG-ES has been reported to be a successful means of removing potassium tablets remaining in the gastrointestinal tract (2,13 15). In our patient, WBI was commenced but was not completed due to combativeness and declining mental status, as the patient was not able to tolerate oral administration and she refused repeated insertion of the NG tube. The change in mental status was believed to be due to coingestion of benzodiazepines. Consideration was given to more aggressive attempts at WBI with airway protection, however, there was concern about the ability of WBI to eliminate the radiographically apparent pharmacobezoar. With this in mind, the decision was made to pursue endoscopic removal. The patient underwent successful removal of a pharmacobezoar with improvement in potassium levels. Serum potassium level of 4.5 mmol/L was obtained approximately 11 h after ED arrival. She was extubated after the procedure and monitored in the intensive care unit. To our knowledge, this is the first report of successful endoscopic removal of a potassium chloride pharmacobezoar. The pharmacobezoar may have increased the risk of the hyperkalemia due to the erratic and prolonged absorption of the potassium. Co-ingestion of substances or drugs that delay gastric emptying like alprazolam may promote bezoar formation. We recommend that in cases of suspected or confirmed potassium drug bezoar in the stomach, physicians consider EGD for removal. This allows for normalization of potassium levels and obviates the need for prolonged intubation to protect the airway in case of prolonged WBI. CONCLUSIONS This was a case of intentional potassium and alprazolam overdose resulting in hyperkalemia with normalization
of potassium levels after utilizing both potassiumlowering medications and EGD. Although intentional overdose with potassium supplementation is rare, bezoar formation can lead to prolonged and erratic absorption of potassium and increase the risk of hyperkalemic sequelae. In addition to standard treatments for hyperkalemia, our case report demonstrates the benefit from EGD in extended-release potassium bezoar formation. REFERENCES 1. John SK, Rangan Y, Block C, Koff M. Life-threatening hyperkalemia from nutritional supplements: uncommon or undiagnosed? Am J Emerg Med 2011;29:1237e1–2. 2. Su M, Stork C, Ravuri S, et al. Sustained-release potassium chloride overdose. Clin Toxicol 2001;39:641–8. 3. Hollander-Rodriguez JC, Calvert JF. Hyperkalemia. Am Fam Phys 2006;73:283–90. 4. Evans KJ, Greenberg A. Hyperkalemia: a review. J Intensive Care Med 2005;20:272–89. 5. Sanders MK. Bezoars: from mystical charms to medical and nutritional management. Pract Gastroenterol 2004;13:37–50. 6. Rogers LR, Wallick D. Reviewing the use of ethylcellulose, methylcellulose and hypromellose in microencapsulation. Part 1: materials used to formulate microcapsules. Drug Dev Indust Pharm 2012;38:129–57. 7. Samyn JC, Jung WY. In vitro dissolution from several experimental capsule formations. J Pharm Sci 1970;59:169–75. 8. Murthy KS, Samyn JC. Effect of shear mixing on in vitro drug development of capsule formulations containing lubricants. J Pharm Sci 1977;66:1215–9. 9. Ng HW, Tse ML, Lau FL, Chu W. Endoscopic removal of iron bezoar following acute overdose. Clin Toxicol 2008;46:913–5. 10. Hojer J, Personne M. Endoscopic removal of slow release clomipramine bezoars in two cases of acute poisoning. Clin Toxicol 2008; 46:317–9. 11. Wells CD, Luckritz TC, Rady MY, et al. Bezoar formation requiring endoscopic removal after intentional overdose of extended-release nifedipine. Pharmacotherapy 2006;26:1802–5. 12. Elliott MJ, Ronksley PE, Clase CM, et al. Management of patients with acute hyperkalemia. CMAJ 2010;182:1631–5. 13. American Academy of Clinical Toxicology. European Association of Poison Centres and Clinical Toxicologists. Position paper: whole bowel irrigation. J Toxicol Clin Toxicol 2004; 42:843–54. 14. Whitaker RJ, Maguire JE. Slow-release potassium overdose: clinical features and the role of whole-bowel lavage in management. Emerg Med 2000;12:218–25. 15. Wan CK, Tong HK. A case of slow-release potassium chloride overdose. Hong Kong J Emerg Med 2007;14:169–73.